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@ARTICLE{Hawwari:284080,
      author       = {Hawwari, Ibrahim and Rossnagel, Lukas and Rosero, Nathalia
                      and Maasewerd, Salie and Vasconcelos, Matilde B and
                      Jentzsch, Marius and Demczuk, Agnieszka and Teichmann, Lino
                      L and Meffert, Lisa and Bertheloot, Damien and Secchim
                      Ribeiro, Lucas and Kallabis, Sebastian and Meissner, Felix
                      and Arditi, Moshe and Atici, Asli E and Noval Rivas, Magali
                      and Franklin, Bernardo S},
      title        = {{P}latelet transcription factors license the
                      pro-inflammatory cytokine response of human monocytes},
      journal      = {EMBO molecular medicine},
      volume       = {16},
      number       = {8},
      issn         = {1757-4676},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2026-00088},
      pages        = {1901 - 1929},
      year         = {2024},
      abstract     = {In humans, blood Classical CD14+ monocytes contribute to
                      host defense by secreting large amounts of pro-inflammatory
                      cytokines. Their aberrant activity causes hyper-inflammation
                      and life-threatening cytokine storms, while dysfunctional
                      monocytes are associated with 'immunoparalysis', a state of
                      immune hypo responsiveness and reduced pro-inflammatory gene
                      expression, predisposing individuals to opportunistic
                      infections. Understanding how monocyte functions are
                      regulated is critical to prevent these harmful outcomes. We
                      reveal platelets' vital role in the pro-inflammatory
                      cytokine responses of human monocytes. Naturally low
                      platelet counts in patients with immune thrombocytopenia or
                      removal of platelets from healthy monocytes result in
                      monocyte immunoparalysis, marked by impaired cytokine
                      response to immune challenge and weakened host defense
                      transcriptional programs. Remarkably, supplementing
                      monocytes with fresh platelets reverses these conditions. We
                      discovered that platelets serve as reservoirs of key
                      cytokine transcription regulators, such as NF-κB and MAPK
                      p38, and pinpointed the enrichment of platelet NF-κB2 in
                      human monocytes by proteomics. Platelets proportionally
                      restore impaired cytokine production in human monocytes
                      lacking MAPK p38α, NF-κB p65, and NF-κB2. We uncovered a
                      vesicle-mediated platelet-monocyte-propagation of
                      inflammatory transcription regulators, positioning platelets
                      as central checkpoints in monocyte inflammation.},
      keywords     = {Humans / Monocytes: metabolism / Monocytes: immunology /
                      Blood Platelets: metabolism / Blood Platelets: immunology /
                      Cytokines: metabolism / Transcription Factors: metabolism /
                      Transcription Factors: genetics / Inflammation: metabolism /
                      Hyperinflammation (Other) / Immune Thrombocytopenia (Other)
                      / Immunoparalysis (Other) / Inflammasomes (Other) /
                      Toll-like Receptors (Other) / Cytokines (NLM Chemicals) /
                      Transcription Factors (NLM Chemicals)},
      ddc          = {610},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1038/s44321-024-00093-3},
      url          = {https://pub.dzne.de/record/284080},
}